mTOR links oncogenic signaling to tumor cell metabolism |
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Authors: | Jessica?L?Yecies Email author" target="_blank">Brendan?D?ManningEmail author |
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Institution: | (1) Department of Genetics and Complex Diseases, Harvard School of Public Health, 665 Huntington Ave, SPH2-117, Boston, MA 02115, USA; |
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Abstract: | As a key regulator of cell growth and proliferation, the mammalian target of rapamycin (mTOR) complex 1 (mTORC1) has been
the subject of intense investigation for its role in tumor development and progression. This research has revealed a signaling
network of oncogenes and tumor suppressors lying upstream of mTORC1, and oncogenic perturbations to this network result in
the aberrant activation of this kinase complex in the majority of human cancers. However, the molecular events downstream
of mTORC1 contributing to tumor cell growth and proliferation are just coming to light. In addition to its better-known functions
in promoting protein synthesis and suppressing autophagy, mTORC1 has emerged as a key regulator of cellular metabolism. Recent
studies have found that mTORC1 activation is sufficient to stimulate an increase in glucose uptake, glycolysis, and de novo
lipid biosynthesis, which are considered metabolic hallmarks of cancer, as well as the pentose phosphate pathway. Here, we
focus on the molecular mechanisms of metabolic regulation by mTORC1 and the potential consequences for anabolic tumor growth
and therapeutic strategies. |
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Keywords: | |
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